scholarly journals Paradoxical role of high mobility group box 1 in glioma: a suppressor or a promoter?

2017 ◽  
Author(s):  
Richard A. Seidu ◽  
Min Wu ◽  
Zhaoliang Su ◽  
Huaxi Xu
Keyword(s):  
Molecular Mechanisms ◽  
High Mobility ◽  
Treatment Resistance ◽  
High Mobility Group ◽  
Tissue Invasion ◽  
Self Sufficiency ◽  
Glycation End Products ◽  
And Migration ◽  
Proliferation And Migration

Gliomas represent 60% of primary intracranial brain tumors and 80% of all malignant types, with highest morbidity and mortality worldwide. Although glioma has been extensively studied, the molecular mechanisms underlying its pathology remain poorly understood. Clarification of the molecular mechanisms involved in their development and/or treatment resistance is highly required. High mobility group box 1 protein (HMGB1) is a nuclear protein that can also act as an extracellular trigger of inflammation, proliferation and migration, through receptor for advanced glycation end products and toll like receptors in a number of cancers including gliomas. It is known that excessive release of HMGB1 in cancer leads to unlimited replicative potential, ability to develop blood vessels (angiogenesis), evasion of programmed cell death (apoptosis), self-sufficiency in growth signals, insensitivity to inhibitors of growth, inflammation, tissue invasion and metastasis. In this review we explore the mechanisms by which HMGB1 regulates apoptosis and autophagy in glioma. We also looked at how HMGB1 mediates glioma regression and promotes angiogenesis as well as possible signaling pathways with an attempt to provide potential therapeutic targets for the treatment of glioma.

The Role of High Mobility Group Box 1 (HMGB1) in Neurodegeneration: A Systematic Review

2022 ◽  
Vol 20 ◽  
Author(s):  
Fathimath Zaha Ikram ◽  
Alina Arulsamy ◽  
Thaarvena Retinasamy ◽  
Mohd. Farooq Shaikh
Keyword(s):  
Systematic Review ◽  
Tissue Injury ◽  
High Mobility ◽  
High Mobility Group ◽  
Hmgb1 Protein ◽  
Toll Like Receptor 4 ◽  
Neuroinflammatory Response ◽  
Molecular Pattern ◽  
Glycation End Products

Background: High mobility group box 1 (HMGB1) protein is a damage-associated molecular pattern (DAMP) molecule that plays an important role in the repair and regeneration of tissue injury. It also acts as a pro-inflammatory cytokine through the activation of toll-like receptor 4 (TLR4) and receptor for advanced glycation end products (RAGE), to elicit the neuroinflammatory response. HMGB1 may aggravate several cellular responses which may lead to pathological inflammation and cellular death. Thus, there have been a considerable amount of research into the pathological role of HMGB1 in diseases. However, whether the mechanism of action of HMGB1 is similar in all neurodegenerative disease pathology remains to be determined. Objective: Therefore, this systematic review aimed to critically evaluate and elucidate the role of HMGB1 in the pathology of neurodegeneration based on the available literature. Methods: A comprehensive literature search was performed on four databases; EMBASE, PubMed, Scopus, and CINAHL Plus. Results: A total of 85 articles were selected for critical appraisal, after subjecting to the inclusion and exclusion criteria in this study. The selected articles revealed that HMGB1 levels were found elevated in most neurodegeneration except in Huntington’s disease and Spinocerebellar ataxia, where the levels were found decreased. This review also showcased that HMGB1 may act on distinctive pathways to elicit its pathological response leading to the various neurodegeneration processes/diseases. Conclusion: While there have been promising findings in HMGB1 intervention research, further studies may still be required before any HMGB1 intervention may be recommended as a therapeutic target for neurodegenerative diseases.

scholarly journals HMBG1 as a Driver of Inflammatory and Immune Processes in the Pathogenesis of Ocular Diseases

2018 ◽  
Vol 2018 ◽  
pp. 1-8
Author(s):  
Yi Liu ◽  
Guo-Bin Zhuang ◽  
Xue-Zhi Zhou
Keyword(s):  
Current Knowledge ◽  
High Mobility ◽  
Retinal Cell ◽  
Ocular Diseases ◽  
Wide Range ◽  
Glycation End Products ◽  
Cell Layers ◽  
Proinflammatory Activity ◽  
And Migration ◽  
Proliferation And Migration

High-mobility group box 1 (HMGB1) is a nuclear protein that can also act as an extracellular trigger of inflammation, proliferation, and migration in eye diseases. It induces signaling pathways by binding to the receptor for advanced glycation end products (RAGE) and Toll-like receptors (TLRs) 2, 4, and 9. This proinflammatory activity is considered to be important in the pathogenesis of a wide range of ocular diseases resulting from hemodynamic changes, presence of neovascular endothelial cells, secretion of intraocular immune factors or inflammation, and apoptosis of retinal cell layers. Further work is needed to elucidate in detail how HMGB1 contributes to ocular disease and how its damaging activity can be modulated. In this review, we summarize current knowledge on HMGB1 as a ligand that can evoke inflammation and immune responses in ocular diseases.

Role of Receptors for Advanced Glycation End Products and High-Mobility Group Box 1 in the Outcome of Human T Cell Lymphotropic Type 1 Infection

2019 ◽  
Vol 32 (2) ◽  
pp. 89-94 ◽  
Author(s):  
Nafise Yaghouti ◽  
Reza Boostani ◽  
Asadollah Mohamamdi ◽  
Zohreh Poursina ◽  
Seyed Abdolrahim Rezaee ◽  
...  
Keyword(s):  
T Cell ◽  
Advanced Glycation End Products ◽  
High Mobility ◽  
High Mobility Group ◽  
Advanced Glycation ◽  
Human T Cell ◽  
Glycation End Products ◽  
End Products

scholarly journals Role of high-mobility group box 1 in methamphetamine-induced activation and migration of astrocytes

2015 ◽  
Vol 12 (1) ◽  
Author(s):  
Yuan Zhang ◽  
Tiebing Zhu ◽  
Xiaotian Zhang ◽  
Jie Chao ◽  
Gang Hu ◽  
...  
Keyword(s):  
High Mobility ◽  
High Mobility Group ◽  
And Migration

scholarly journals Emerging Role of High Mobility Group Box-1 in Thrombosis-Related Diseases

2018 ◽  
Vol 47 (4) ◽  
pp. 1319-1337 ◽  
Author(s):  
Han Wu ◽  
Ran Li ◽  
Li-Gang Pei ◽  
Zhong-Hai Wei ◽  
Li-Na Kang ◽  
...  
Keyword(s):  
High Mobility ◽  
Arterial Disease ◽  
High Mobility Group ◽  
Toll Like Receptor 4 ◽  
Close Link ◽  
Molecular Pattern ◽  
Glycation End Products ◽  
Artery Disease ◽  
Peripheral Arterial

High mobility group box-1 (HMGB-1), a typical damage-associated molecular pattern protein released from various cells, was first identified in 1973. It is usually stored in the nuclei of cells. Several modifications of HMGB-1 promote its translocation to the cytosol, and it is actively or passively released from cells. When outside of the cells, HMGB-1is crucial in inflammation. It exerts its biological functions via interaction with its receptors, including receptor for advanced glycation end products (RAGE) and Toll-like receptor 4(TLR4). A large number of studies showed a close link between inflammation and thrombosis. This review demonstrated the increased expression of HMGB-1 in thrombosis-related diseases, including coronary artery disease, stroke, peripheral arterial disease, disseminated intravascular coagulation, and venous thrombosis. Besides, it summarized the current understanding of the emerging link between HMGB-1 and thrombosis from three aspects: platelet, NETs, and coagulation and fibrinolysis factors. Finally, it explored the possible therapeutic strategies targeting HMGB-1 for treating thrombosis-related diseases.

scholarly journals Mechanism of resistin-induced enhancement of proliferation and migration of ovarian cancer cells

2020 ◽  
Author(s):  
Li Pang ◽  
Xian-li Li
Keyword(s):  
Ovarian Cancer ◽  
Wound Healing ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Ovarian Cancer Cells ◽  
Dependent Manner ◽  
Ovarian Epithelial Carcinoma ◽  
And Migration ◽  
Proliferation And Migration

IntroductionResistin, a novel hormone secreted by human adipocytes and mononuclear cells, is associated with obesity, insulin resistance, and inflammation. Recent studies showed that resistin plays a key role in ovarian cancer cells. In this study, we investigated the potential of resistin to regulate the proliferation and migration of ovarian cancer cells.Material and methodsA series of in vitro functional experiments were carried out to elucidate the role of resistin in ovarian cancer progression and the molecular mechanisms underlying its role.ResultsResistin enhanced the proliferation of human ovarian epithelial carcinoma cells (HO-8910) in a time- and dose-dependent manner (30–100 ng/ml). Furthermore, HO-8910 cells cultured in adipocyte-conditioned medium showed dramatically increased rates of proliferation. Resistin knockout during adipocyte culture attenuated the proliferation of HO-8910 cells treated with adipocyte-conditioned media, indicating that resistin may promote HO-8910 cell proliferation via the mechanistic target of a rapamycin (mTOR)-mediated signaling pathway. Resistin (30–100 ng/ml) also enhanced wound-healing rates in a time- and concentration-dependent manner. Co-culturing HO-8910 cells with adipocytes also increased the wound-healing rates. Resistin expression was inhibited by miR-124-1 transcriptional activity, and resistin-mediated HO-8910 cell migration was also regulated by miR-124-1. Furthermore, we also confirmed the role of resistin in promoting tumor growth in vivo.ConclusionsThese findings suggest that resistin may serve as an effective therapeutic target for ovarian epithelial carcinoma, especially in patients who are obese.

scholarly journals CLIC1 facilitates cancer associated fibroblast activation and gastric cancer progression via integrins/NF-κB pathway

2020 ◽  
Author(s):  
Min Meng ◽  
Hong-Bo Wang ◽  
Su-Zhen Song ◽  
Rong Sun ◽  
Yu Lin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Neutralizing Antibodies ◽  
Molecular Mechanisms ◽  
Stem Cell Markers ◽  
Cancer Stem Cell Markers ◽  
Cancer Associated Fibroblast ◽  
And Migration ◽  
Proliferation And Migration

Background: Gastric cancer (GC) is one of the most common and lethal cancers and the prognosis of GC patients remains very poor. Cancer-associated fibroblasts (CAFs) largely facilitate the progression of GC but the underlying molecular mechanisms remain elusive despite numerous studies. Here, we investigated the role of CLIC1 in CAF activation and GC. Methods: qRT-PCR and western blot were performed to determine expression levels of cytokines, transcription factors and related proteins such as CAF markers. MTT assay was used to examine the proliferation of GC cells while transwell assay and tumorsphere formation assay were done to measure the migration, invasion and stemness of GC cells. Conditioned medium model was used to examine the intercellular communication between CAFs and GC cells. Results: Overexpression of CLIC1 in fibroblasts induced CAF activation and enhanced cell proliferation and migration. Also, CLIC1 up-regulated integrins/NF-κB signaling in CAFs. CLIC1-overexpressed fibroblasts promoted proliferation and migration of GC cells and up-regulated cancer stem cell markers and promoted EMT program of GC cells. IL-6 and IL-8 neutralizing antibodies inhibit the pro-tumor effects of CLIC1-overexpressing fibroblasts on GC cells. Further, knockdown CLIC1 in GC cells suppressed activation of CAF. Conclusions: CLIC1 overexpression activates CAF via up-regulating integrins/NF-κB signaling and activated CAF releases IL-6 and IL-8 to promote multiple malignant phenotypes of GC cells. These results implicate an essential role of CLIC1 in CAF activation and GC progression, which suggests that CLIC1 could serve as a potential target for GC therapy.

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